Search results for " UPR"

showing 10 items of 484 documents

Expression pattern of the urokinase-plasminogen activator system in rat DS-sarcoma: Role of oxygenation status and tumour size

2002

The urokinase plasminogen activator system plays a central role in malignant tumour progression. Both tumour hypoxia and enhancement of urokinase plasminogen activator, urokinase plasminogen activator-receptor and plasminogen activator inhibitor type 1 have been identified as adverse prognostic factors. Upregulation of urokinase plasminogen activator or plasminogen activator inhibitor type 1 could present means by which hypoxia influences malignant progression. Therefore, the impact of hypoxia on the expression pattern of the urokinase plasminogen activator system in rat DS-sarcoma in vivo and in vitro was examined. In the in vivo setting, tumour cells were implanted subcutaneously into rat…

Cancer Researchplasminogen activator inhibitor type-1DS-sarcomaEnzyme-Linked Immunosorbent AssayReceptors Cell Surfaceurokinase plasminogen activator receptorBiologyReceptors Urokinase Plasminogen Activatorchemistry.chemical_compoundDownregulation and upregulationIn vivoPlasminogen Activator Inhibitor 1Tumor Cells CulturedmedicineAnimalsExperimental TherapeuticsZymographyRNA Messengerurokinase plasminogen activatorHyperoxiaUrokinasehypoxiaReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingSarcomamalignant progressionUrokinase-Type Plasminogen ActivatorMolecular biologyIn vitroRatsGene Expression Regulation NeoplasticOxygenUrokinase receptorOncologychemistryOrgan SpecificityPlasminogen activator inhibitor-1medicine.symptommedicine.drugBritish Journal of Cancer
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MYC dosage compensation is mediated by miRNA-transcription factor interactions in aneuploid cancer

2021

Summary We hypothesize that dosage compensation of critical genes arises from systems-level properties for cancer cells to withstand the negative effects of aneuploidy. We identified several candidate genes in cancer multiomics data and developed a biocomputational platform to construct a mathematical model of their interaction network with micro-RNAs and transcription factors, where the property of dosage compensation emerged for MYC and was dependent on the kinetic parameters of its feedback interactions with three micro-RNAs. These circuits were experimentally validated using a genetic tug-of-war technique to overexpress an exogenous MYC, leading to overexpression of the three microRNAs …

Candidate geneMultidisciplinaryDosage compensationColorectal cancerBioinformaticsScienceQCancerMycBiologymedicine.diseaseArticleDownregulation and upregulationCancer cellmicroRNATranscription factorsmedicineCancer researchcancerDosage compensationaneuploidyMathematical biosciencesSystems biologyTranscription factormiRNAiScience
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WIN55,212-2-induced expression of Mir-29b1 favours the suppression of osteosarcoma cell migration in a SPARC-independent manner

2019

WIN55,212-2 (WIN) is a synthetic agonist of cannabinoid receptors that displays promising antitumour properties. The aim of this study is to demonstrate that WIN is able to block the migratory ability of osteosarcoma cells and characterize the mechanisms involved. Using wound healing assay and zymography, we showed that WIN affects cell migration and reduces the activity of the metalloproteases MMP2 and MMP9. This effect seemed to be independent of secreted protein acidic and rich in cysteine (SPARC), a matricellular protein involved in tissue remodeling and extracellular matrix deposition. SPARC release was indeed prevented by WIN, and SPARC silencing by RNA interference did not influence …

Cannabinoid receptorMorpholinesAntineoplastic AgentsMMP9NaphthalenesCatalysisArticlelcsh:ChemistryInorganic ChemistryExtracellular matrixExtracellular VesiclescannabinoidsDownregulation and upregulationCell MovementCell Line TumorSettore BIO/10 - BiochimicaGene silencingHumansOsteonectinCell migrationPhysical and Theoretical Chemistrylcsh:QH301-705.5Molecular BiologyCannabinoidSpectroscopyCell ProliferationOsteosarcomaChemistryCell growthOrganic ChemistryMatricellular proteinCell migrationSPARCGeneral MedicineComputer Science ApplicationsCell biologyBenzoxazinesMiR-29b1MicroRNAslcsh:Biology (General)lcsh:QD1-999
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Analysis of Possible Mechanisms Accounting for Raf-1 Kinase Inhibitor Protein Downregulation in Hepatocellular Carcinoma

2012

Abstract Raf-1 kinase inhibitor protein (RKIP) is a tumor and metastasis suppressor that promotes drug-induced apoptosis in cancer cells. It is frequently downregulated, both at the mRNA and protein level, in hepatocellular carcinoma (HCC), but the mechanisms leading to this reduction are obscure. We sequenced the whole RKIP gene in three human HCC cell lines (HA22T/VGH, HepG2, and Hep3B), and in five clinical HCC samples, but could not find any gene variant that might account for their low RKIP levels. We also examined whether gene methylation may be responsible for the altered RKIP expression. No methylation of the RKIP gene was found in the tumor samples, while among the cell lines only …

Carcinoma HepatocellularLeupeptinsAntineoplastic AgentsPhosphatidylethanolamine Binding ProteinRKIP (Raf-1 kinase inhibitor protein) hepatocellular carcinomaBiologyBiochemistryDownregulation and upregulationRNA interferenceCell Line TumorGeneticsHumansMetastasis suppressorPromoter Regions GeneticMolecular BiologyRegulation of gene expressionKinaseLiver NeoplasmsHep G2 CellsMethylationDNA Methylationdigestive system diseasesGene Expression Regulation NeoplasticMicroRNAsMutationCancer cellDNA methylationAzacitidineSettore BIO/14 - FarmacologiaCancer researchMolecular MedicineRNA InterferenceBiotechnologyOMICS: A Journal of Integrative Biology
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miR-133a Enhances the Protective Capacity of Cardiac Progenitors Cells after Myocardial Infarction

2014

Summary miR-133a and miR-1 are known as muscle-specific microRNAs that are involved in cardiac development and pathophysiology. We have shown that both miR-1 and miR-133a are early and progressively upregulated during in vitro cardiac differentiation of adult cardiac progenitor cells (CPCs), but only miR-133a expression was enhanced under in vitro oxidative stress. miR-1 was demonstrated to favor differentiation of CPCs, whereas miR-133a overexpression protected CPCs against cell death, targeting, among others, the proapoptotic genes Bim and Bmf. miR-133a-CPCs clearly improved cardiac function in a rat myocardial infarction model by reducing fibrosis and hypertrophy and increasing vasculari…

Cardiac function curveProgrammed cell deathMyocardial InfarctionGene ExpressionCardiomegalyBiologyBiochemistryArticleMuscle hypertrophyParacrine signallingDownregulation and upregulationmiR-133a; Cardiac Progenitors Cells; Myocardial InfarctionFibrosisREGENERATIONmicroRNAGeneticsmedicineMyocyteAnimalsRNA MessengerOXIDATIVE STRESSlcsh:QH301-705.5ENGINEERED HEART-TISSUElcsh:R5-920Gene Expression ProfilingMICRORNAComputational BiologyCell BiologyMUSCLEmedicine.disease3. Good healthCell biologyRatsAPOPTOSISHYPERTROPHYMicroRNAsDIFFERENTIATIONlcsh:Biology (General)ImmunologyGROWTHRNA Interferencelcsh:Medicine (General)EMBRYONIC STEM-CELLSMyoblasts CardiacDevelopmental BiologyStem Cell Reports
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Expression of Gelatinases (MMP-2, MMP-9) in human articular cartilage

2013

Osteoarthritis (OA) is a chronic degenerative joint disorder characterized by destruction of the articular cartilage, subchondral bone alterations and synovitis. Matrix metalloproteinases (MMPs) are expressed in joint tissues of patients with osteoarthritis (OA). The objective of this study was to define the steady state levels of two different MMPs to provide more insight into the role of MMPs in cartilage destruction in OA. We investigated the expression of gelatinases through immunohistochemistry Our results show that high levels of MMP-2 and MMP-9 are present in OA and suggest that once these MMPs are fully activated they may contribute to the cartilage destruction in OA.

Cartilage ArticularSettore BIO/17 - IstologiaGelatinasesPathologymedicine.medical_specialtyImmunologyArticular cartilage; Metalloproteinases; Immunohistochemistry; OsteoarthritisArticular cartilageOsteoarthritisMatrix metalloproteinaseArticular cartilageOsteoarthritis HipDownregulation and upregulationSynovitisOsteoarthritisHumansImmunology and AllergyMedicineMetalloproteinasePharmacologybusiness.industryCartilageAnatomyOsteoarthritis Kneemedicine.diseaseImmunohistochemistryUp-Regulationmedicine.anatomical_structureMatrix Metalloproteinase 9Case-Control StudiesMatrix Metalloproteinase 2Immunohistochemistrybusiness
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Toll-like receptor 3 mediates expression of clusterin/apolipoprotein J in vascular smooth muscle cells stimulated with RNA released from necrotic cel…

2010

Clusterin/Apolipoprotein J is a protein that is upregulated in a broad spectrum of diverse pathological processes. The predominant form is a secreted glycoprotein (sCLU) with cytoprotective and anti-inflammatory properties which shows enhanced expression in vascular smooth muscle cells (VSMC) following aortic injury and in atherosclerotic disease. Recent evidence indicates that during atherosclerosis, Toll-like receptors (TLRs) are activated in vascular cells by endogenous ligands. Here, we analyzed whether CLU expression in VSMC is controlled by TLRs, and stimulated by factors associated with or released by necrotic cells. Activation of TLR3 by the synthetic RNA analogue polyinosinic-polyc…

Cell ExtractsProtein DenaturationHot TemperatureMyocytes Smooth MuscleMedizinGene ExpressionBiologyTransfectionMuscle Smooth VascularCell LineMiceNecrosisDogsDownregulation and upregulationGene expressionAnimalsHumansChemokine CCL2Mice KnockoutMessenger RNAToll-like receptorClusterinToll-Like ReceptorsProteinsChloroquineCell BiologyMolecular biologyEndocytosisRatsToll-Like Receptor 3Mice Inbred C57BLTLR2Adaptor Proteins Vesicular TransportClusterinPoly I-CCulture Media ConditionedTLR3biology.proteinRNAEctopic expressionExperimental cell research
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mRNA-induction and cytokine release during in vitro exposure of human nasal respiratory epithelia to methyl methacrylate

2007

Abstract Background Methyl methacrylate (MMA) has been reported to cause histopathological changes in rodent nasal epithelium after inhalation challenges. Data in humans are lacking. Methods In this in vitro design 22 primary cell cultures taken from inferior turbinate tissue of healthy individuals were exposed to MMA concentrations of 50 ppm (German MAK-value) and 200 ppm. mRNA expression and cytokine release of inflammatory mediators were quantified after 4 h and after 24 h. Controls were exposed to synthetic air. Q-PCR analysis was performed for TNF-α, IL-1β, IL-6, IL-8, MCP-1, GMCSF, Cox-1 and Cox-2. ELISA assays were performed from culture supernatants for TNF-α, IL-1β, IL-6, IL-8, MCP…

Cell Survivalmedicine.medical_treatmentCell Culture TechniquesEnzyme-Linked Immunosorbent AssayInflammationMethylmethacrylateBiologyToxicologyAndrologyDownregulation and upregulationmedicineHumansRNA MessengerRespiratory systemCells CulturedChemokine CCL2Dose-Response Relationship DrugReverse Transcriptase Polymerase Chain ReactionTumor Necrosis Factor-alphaInterleukinsGranulocyte-Macrophage Colony-Stimulating FactorAntimutagenic AgentsEpithelial CellsGeneral MedicineEpitheliumIn vitroNasal MucosaDose–response relationshipCytokinemedicine.anatomical_structureGene Expression RegulationCyclooxygenase 2Cell cultureImmunologyCyclooxygenase 1Cytokinesmedicine.symptomToxicology Letters
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Down-regulation of nuclear binding activities of OXBOX-REBOX transcription factors during cellular senescence.

1996

Functional capacity of mitochondria declines during aging and this impairment may have a major role in aging process. Several observations indicate that transcriptional efficiency is reduced during aging. Our purpose was to find out whether aging and cellular senescence affect the nuclear binding activities of transcription factors which bind to OXBOX-REBOX sequence present in promoter regions of numerous nuclear genes encoding mitochondrial proteins. These factors regulate and coordinate the expression of mitochondrial proteins. We observed a strong down-regulation in the nuclear binding activities of OXBOX-REBOX factors in replicatively senesced human WI-38 and IMR-90 fibroblasts. On the …

Cell cycle checkpointNuclear genePhotoagingMolecular Sequence DataBiophysicsDown-RegulationPlasma protein bindingBiologyMitochondrionBiochemistryDownregulation and upregulationmedicineAnimalsHumansRats WistarMolecular BiologyTranscription factorCellular SenescenceCell Line TransformedBase SequenceNuclear ProteinsCell BiologyDNAmedicine.diseaseCell biologyRatsCell cultureProtein BindingTranscription FactorsBiochemical and biophysical research communications
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All-trans retinoic acid restores gap junctional intercellular communication between oral cancer cells with upregulation of Cx32 and Cx43 expressions …

2012

Objective: All-trans retinoic acid (ATRA) has been demonstrated to inhibit tumor growth by restoration of gap junctional intercellular communication (GJIC) via upregulation of connexin (Cx) expression in some solid tumors. However, the relationship between ATRA and GJIC remains unclear in oral squamous cell carcinoma (OSCC). The aim of this study was to investigate the effect of ATRA on the GJIC function of OSCC. Study design: We measured the effects of ATRA on the viability and cell cycle distribution of SCC9 and Tca8113 OSCC cells. The GJIC function was observed using the scrape-loading dye transfer technique, and the mRNA and protein levels of Cx32 and Cx43 were detected by qRT-PCR, West…

Cell cycle checkpointRetinoic acidConnexinAntineoplastic AgentsTretinoinOdontologíaCell CommunicationConnexinschemistry.chemical_compoundDownregulation and upregulationTretinoinmedicineTumor Cells CulturedHumansRNA MessengerGeneral DentistryneoplasmsMouth neoplasmOral Medicine and Pathologyorganic chemicalsGap JunctionsCell cycle:CIENCIAS MÉDICAS [UNESCO]Ciencias de la saludbiological factorsUp-RegulationGene Expression Regulation Neoplasticstomatognathic diseasesOtorhinolaryngologychemistryConnexin 43ImmunologyCancer cellUNESCO::CIENCIAS MÉDICASCancer researchCarcinoma Squamous CellSurgeryMouth NeoplasmsResearch-Articlemedicine.drug
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